Nephrology Flashcards
goserelin - action & other name?
GnRH agonist
zoladex
locally advanced prostate cancer
spike and dome appearance on EM - what dx?
membranous GN
anti-phospholipase a2 antibodies what dx?
membranous GN
why is nephrotic syndrome hypercoagulable
loss of antithrombin 3 from kidneys
why does ckd cause anaemia
due to reduced levels of EP
whats most common cause of peritonitis 2o to peritoneal dialysis
coag negative staph eg epidermis, capitis
2nd most common: staph aureus (coag +ve)
sterile pyuria and white cell casts with rash + fever
Acute interstitial nephritis
- Commonly due to abx
Features
- Fever, rash, arthralgia - Eosinophilia - Mild renal impairment - HTN
Histo: marked interstitial oedema + interstitial infiltrate in connective tissue between renal tubules
+ve congo-red stain - when polarised light shone, it appears apple green
amyloidosis
tx for AD PKD?
tolvaptan = vasopressin rec 2 antag
GNs that present with nephritic syn
Rapidly progressive GN
- goodpasture’s, anca positive vasculitis/wegener’s
IgA nephropathy/berger’s/mesangioproliferative GN
Alport syndrome
what presents with a mixed nephritic/nephrotic pic
Diffuse proliferative GN
- Post-strep GN in child - Nephritic syn/AKI - Most common form of renal disease in SLE
Membranoproliferative GN (mesangiocapillary)
- Type 1: cryoglobinaemia, hep C
Type 2: partial lipodystrophy
what presents w nephrotic syndrome
Minimal change disease
- Child w nephrotic syn - Causes: hodgkin's, NSAIDs - Good response to steroids
Membranous GN
- Proteinuria/nephrotic syn/CKD - Causes infections, rheumatoid drugs, cancer - 1/3 resolve, 1/3 respond to cytotoxics, 1/3 ckd
FSGS
- idiopathic, or due to HIV/heroin
Proteinuria/nephrotic syn/ckd
young women who dev AKI after starting ACEi
Fibromuscular dysplasia: consider in young women who dev AKI after starting ACEi
Renal artery stenosis: old = atherosclerosis. Young F = FMD
upper resp tract signs (recurrent sinusitis), nosebleeds, saddle-shaped nose, vasculitic rash
granulomatosis w polyangiitis
haemoptysis
Goodpasture’s: haemoptysis
Crescentic GN
lower resp symptoms EG recent dx asthma, eosinophilia on bloods
Eosinophilic granulomatosis w polyangiitis
young pt w macroscpoic haematuria just after an acute upper rest infection
IgA nephropathy
enlarged and hypercellular glomeruli w starry sky (granular)
Post-strep GN:
Microscopic haematuria, bilateral SN deafness, progressive renal failure, longitudinal splitting of lamina densa of GBM on EM (basket weave appearance)
Alport’s:
• X-linked dominant
• Defect in gene for type IV collagen > abnormal GBM
• Failing renal transplant – anti-GBM Abs»_space; goodpasture’s picture
• Microscopic haematuria, bilateral SN deafness, progressive renal failure, longitudinal splitting of lamina densa of GBM on EM (basket weave appearance)
• More severe in M (women rarely get renal failure)
stag horn calculi - made of?
Stag horn calculi: struvite
(ammonium, magnesium, phosphate; triple phosphate)
form in alkaline urine
- so ammonia producing bacteria eg ureaplasma and proteus predispose to it
tx of BPH?
- if mod-severe voiding symptoms = alpha-1 antags (tamsulosin, alfuzosin)
• SE: dizzy, postural hypotension, dry mouth, depressed
• If persistent can add in tolterodine, darifenacin (anticholingeric/antimuscarinic) - if sig enlarged prostate and at high risk of progression: finasteride (5 alpha reductase inhibitor) - takes 6 months to work but slows disease progression
- SE: erectile dysfunction, reduced libido, ejaculation problems, gynaecomastia
If both – use both together
Or: TURP
how does chemotx cause kidney disease
hyperuricaemia
what effect does alcohol binge drinking have on the kidneys
Alcohol binge drinking can > ADH suppression in posterior pit gland > polyuria
• Hypernatraemia, raised serum osm, low urine osm
Bicalutamide
Bicalutamide: androgen receptor blocker. Used in prostate cancer
bladder problems in M
- mainly voiding syms:
- mixed voiding and storage?
- mainly overactive bladder?
Mainly voiding syms in M: conservative. If mod: a-blocker. If big prostate/high risk: 5-a reductase inhibitor. If both: have both drugs
• If mixed voiding and storage not responding to a-blocker, add antimuscarinic
Mainly overactive bladder in M: conservative. If persist: antimusc (oxybutynin, tolterodine, darifenacin) if fail: mirabegron
GN & low complement (4)
- Post strep GN
- Subacute bacterial endocarditis
- SLE
mesangiocapillary GN
most common histo pattern in lupus nephritis
diffuse proliferative GN
causes of cranial DI
& tx
Cranial: desmopressin
Causes of cranial DI • idiopathic • post head injury • pituitary surgery • craniopharyngiomas • histiocytosis X • DIDMOAD/wolfram's syndrome - Haemochromatosis
nephrogenic DI
causes
tx
Causes of nephrogenic DI
• genetic: ADH rec (more common),aquaporin 2 channel
• electrolytes: high calcium, low K
• lithium
• demeclocycline
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
nephrogenic: thiazides, low salt/protein diet
alport's syndrome - inheritence gene defect features renal biopsy ft
alport's syndrome - inheritence gene defect features renal biopsy ft
ost: x-linked dominant
· defect in the gene which codes for type IV collagen»_space; abnormal GDM
· More severe in M (females rarely get renal failure)
NB renal transplants often fail: due to anti-GBM Abs > goodpasture’s like pic
Usually presents in children • microscopic haematuria • progressive renal failure • bilateral SN deadness • lenticonus: protrusion of the lens surface into the anterior chamber • retinitis pigmentosa
EM: basket-weave (longitudinal splitting of lamina densa of GBM)
DETAILS
Diagnosis
• molecular genetic testing
• renal biopsy
NB 10-15% autosomal recessive
HOW TO TELL ATN FROM AIN ON URINE DIP
Urine dip can differentiate ATN from acute interstitial nephritis:
- AIN: inflam process = more white cells in urine (can be caused by penicillin abx) - ATN: not inflam - no white cells - If protein is present = rules out pre or post renal cause
stages of diabetic nephropathy
Stage 1
• hyperfiltration: increase in GFR
• may be reversible
Stage 2 (silent or latent phase) • most patients do not develop microalbuminuria for 10 years • GFR remains elevated
Stage 3 (incipient nephropathy) • microalbuminuria (albumin excretion of 30 - 300 mg/day, dipstick negative)
Stage 4 (overt nephropathy)
• persistent proteinuria (albumin excretion > 300 mg/day, dipstick positive)
• hypertension is present in most patients
• histology shows diffuse glomerulosclerosis and focal glomerulosclerosis (Kimmelstiel-Wilson nodules)
Stage 5
• end-stage renal disease, GFR typically < 10ml/min
• renal replacement therapy needed
The timeline given here is for type 1 diabetics.
T2DM progress through similar stages but in a different timescale - some T2DM patients may progress quickly to the later stages
how does alcohol cause polyuria
Alcohol binge > ADH suppression in posterior pituitary gland > polyuria
renal stones
- radiolucent (2)
- semi opaque (1)
opaque (4)
radiolucent: urate, xanthine stones
semi opaque: cystine
opaque: calcium oxalate, calcium phosphate, triple phosphate/struvite, mixed ca oxalate/phosphate stones
membranoproliferative GN
- mx?
- types and their causes/fts
· may present as nephrotic syndrome, haematuria or proteinuria
· poor prognosis
Management: steroids may be effective
Type 1 (90%) · cause: cryoglobulinaemia, hep C · EM: subendothelial + mesangium immune deposits of electron-dense material = 'tram-track' appearance
Type 2 - ‘dense deposit disease’
· causes: partial lipodystrophy (loss of SC tissue from face), factor H deficiency
· caused by persistent activation of alternative complement pathway
· low circulating levels of C3
· C3b nephritic factor in 70%
○ an antibody to alternative-pathway C3 convertase (C3bBb)
○ stabilizes C3 convertase
· renal biopsy
○ EM: intramembranous immune complex deposits with ‘dense deposits’
Type 3 causes: hepatitis B and C
metabolic acidosis
- anion gap eqn
- normal range for anion gap
- normal anion gap MA causes (5)
- raised causes (4)
Classified according to the anion gap
- calculated by: (Na+ + K+) - (Cl- + HCO-3) - If a question supplies the chloride level then this is often a clue that the anion gap should be calculated - normal range = 10-18 mmol/L
Normal anion gap ( = hyperchloraemic metabolic acidosis)
• GI bicarb loss: diarrhoea, ureterosigmoidostomy, fistula
• renal tubular acidosis
• drugs: e.g. acetazolamide
• ammonium chloride injection
• Addison’s disease
Raised anion gap • lactate: shock, sepsis, hypoxia • ketones: diabetic ketoacidosis, alcohol • urate: renal failure • acid poisoning: salicylates, methanol
Metabolic acidosis secondary to high lactate levels may be subdivided into two types:
• lactic acidosis type A: sepsis, shock, hypoxia, burns
• lactic acidosis type B: metformin
ATN v prerenal uraemia
Prerenal uraemia - kidneys hold on to sodium to preserve volume
- Fractional sodium excretion <1%, urine sodium <20
High calcium in urine & kidney stones
thiazide diuretics
plasma exchange
indications (7)
comps (5)
Indications for plasma exchange (also known as plasmapheresis)
• GBS
• myasthenia gravis
• Goodpasture’s
• ANCA positive vasculitis if rapidly progressive renal failure or pulmonary haemorrhage
• TTP/HUS
• cryoglobulinaemia
• hyperviscosity syndrome e.g. secondary to myeloma
Complications of plasma exchange • Low calcium • metabolic alkalosis • removal of systemic medications • coagulation factor depletion immunoglobulin depletion
